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线粒体DNA缺失HepG2细胞系的建立、鉴定及放射生物学特性

孙恒文 潘燚 曾子君 方良毅 张红丹 谢松喜 李伟雄 许家彬

南方医科大学学报Issue(6):783-788,6.
南方医科大学学报Issue(6):783-788,6.

线粒体DNA缺失HepG2细胞系的建立、鉴定及放射生物学特性

Observation of radiobiological characteristics in a HepG2 cell line with mitochondrial DNA deletion

孙恒文 1潘燚 1曾子君 1方良毅 1张红丹 1谢松喜 1李伟雄 1许家彬2

作者信息

  • 1. 广东省人民医院//广东省医学科学院肿瘤中心放疗科,广东 广州 510080
  • 2. 广东医学院附属彭湃纪念医院肿瘤科,广东 海丰 516400
  • 折叠

摘要

Abstract

Objective To study the radiobiological characteristics of a HepG2 cell line with mitochondrial DNA (mtDNA) deletion. Methods HepG2 cells were cultured in a medium containing ethidium bromide, acetylformic acid and uracil. The HepG2 cell line with mtDNA deletion (ρ0HepG2 cells) were acquired after 30 subcultures by limited dilution cloning. The cell survival was then observed in the absence of acetylformic acid and uracil, and the total mtDNA deletion in the cells was confirmed by PCR. The radiosensitivity of HepG2 andρ0HepG2 cells was evaluated by exposure to gradient doses of 6 MV X ray irradiation. The cell apoptosis was assessed following a 2 Gy X-ray exposure with Hochest33342 staining, and the invasiveness of ρ0HepG2 cells was measured by Transwell assay. Results HepG2 cells could survive 30 subcultures in the presence of ethidium bromide, and massive cell death occurred after removal of acetylformic acid and uracil from the medium. PCR confirmed total mtDNA deletion fromρ0HepG2 cells, whoseα/βvalue was significantly lower than that of HepG2 cells.ρ0Hep-G2 cells showed an obviously lowered cell apoptosis rate following X-ray exposure with enhanced cell invasiveness. Conclusion HepG2 cells can be induced by ethidium bromide intoρ0HepG2 cells with an increased radiation resistance, anti-apoptosis ability and cell invasiveness.

关键词

辐射敏感性/HepG2/Rho0cells/凋亡

Key words

radiosensitivity/HepG2/Rho0 cells/apoptosis

引用本文复制引用

孙恒文,潘燚,曾子君,方良毅,张红丹,谢松喜,李伟雄,许家彬..线粒体DNA缺失HepG2细胞系的建立、鉴定及放射生物学特性[J].南方医科大学学报,2015,(6):783-788,6.

基金项目

国家自然科学基金(81302033) Supported by National Natural Science Foundation of China (81302033) (81302033)

南方医科大学学报

OA北大核心CSCDCSTPCDMEDLINE

1673-4254

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